SCN5A gene mutations and the risk of ventricular fibrillation and syncope in brugada syndrome patients: A meta‐analysis

Sunu Budhi Raharjo, Rido Maulana, Irma Maghfirah, Fatimah Alzahra, Agnes Dinar Putrinarita, Dicky A. Hanafy, Yoga Yuniadi

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10 Citations (Scopus)


Mutations in the gene encoding the main cardiac sodium channel (SCN5A) are the commonest genetic cause of Brugada syndrome (BrS). However, the effect of SCN5A mutations on the outcomes of ventricular fibrillation (VF) and syncope remains uncertain. To clarify this relationship, a meta‐analysis was performed. A comprehensive search was conducted to identify all eligible studies from PubMed, MEDLINE, EBSCO, ProQuest, Science Direct, Clinical Key, and Cochrane database for cohort studies of BrS populations that had been systematically tested for SCN5A mutations. We did meta‐analysis to see the relationship between SCN5A mutations and the occurrence of VF and/or syncope using RevMan 5.3. Five clinical studies met our criteria and included a total of 665 BrS patients. These studies included 45 patients with VF and 178 patients with syncope. We found that in BrS patients with SCN5A mutations the rate of VF event was 30.7% while in patients without mutations was 28.5% (Risk Ratio [RR] = 1.11, [95% CI: 0.61, 2.00], P = 0.73, I 2 = 0%). The occurrence of syncope events was 35.9% in patients with SCN5A mutations and 34.5% in patients without mutations (RR = 1.12, [95% CI: 0.87, 1.45], P = 0.37, I 2 = 39%). Furthermore, the occurrence of combined VF and syncope events were similar between the 2 groups (RR = 1.12, [95% CI: 0.89, 1.42], P = 0.34, I 2 = 11%). BrS patients with SCN5A mutations exhibit a similar risk of future occurence of VF and/or syncope as compared to those without SCN5A mutations.

Original languageEnglish
Pages (from-to)473-477
Number of pages5
Journaljournal of arrhythmia
Issue number5
Publication statusPublished - 1 Jan 2018


  • Brugada syndrome
  • SCN5A mutations
  • Sodium channel
  • Syncope
  • Ventricular fibrillation


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